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Welcome to The Visible Embryo, a comprehensive educational resource on human development from conception to birth.

The Visible Embryo provides visual references for changes in fetal development throughout pregnancy and can be navigated via fetal development or maternal changes.

The National Institutes of Child Health and Human Development awarded Phase I and Phase II Small Business Innovative Research Grants to develop The Visible Embryo. Initally designed to evaluate the internet as a teaching tool for first year medical students, The Visible Embryo is linked to over 600 educational institutions and is viewed by more than one million visitors each month.

Today, The Visible Embryo is linked to over 600 educational institutions and is viewed by more than 1 million visitors each month. The field of early embryology has grown to include the identification of the stem cell as not only critical to organogenesis in the embryo, but equally critical to organ function and repair in the adult human. The identification and understanding of genetic malfunction, inflammatory responses, and the progression in chronic disease, begins with a grounding in primary cellular and systemic functions manifested in the study of the early embryo.

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Pregnancy Timeline by SemestersFetal liver is producing blood cellsHead may position into pelvisBrain convolutions beginFull TermWhite fat begins to be madeWhite fat begins to be madeHead may position into pelvisImmune system beginningImmune system beginningPeriod of rapid brain growthBrain convolutions beginLungs begin to produce surfactantSensory brain waves begin to activateSensory brain waves begin to activateInner Ear Bones HardenBone marrow starts making blood cellsBone marrow starts making blood cellsBrown fat surrounds lymphatic systemFetal sexual organs visibleFinger and toe prints appearFinger and toe prints appearHeartbeat can be detectedHeartbeat can be detectedBasic Brain Structure in PlaceThe Appearance of SomitesFirst Detectable Brain WavesA Four Chambered HeartBeginning Cerebral HemispheresFemale Reproductive SystemEnd of Embryonic PeriodEnd of Embryonic PeriodFirst Thin Layer of Skin AppearsThird TrimesterSecond TrimesterFirst TrimesterFertilizationDevelopmental Timeline
CLICK ON weeks 0 - 40 and follow along every 2 weeks of fetal development
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Home | Pregnancy Timeline | News Alerts |News Archive Jan 20, 2014

 

Above: Bacteria (singular: bacterium) are unicellular microorganisms typically a few
micrometers long in many shapes including curved rods, spheres, rods, and spirals.

A virus (from the Latin noun virus, meaning toxin or poison) is a sub-microscopic particle
(ranging from 20 to 300 nm) that can infect the cells of any biological organism.

Listeria monocytogenes bacteria. Image Credit: Helmholtz-HZI/Manfred Rohde


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WHO Child Growth Charts

 

 

 

Key difference in response to viruses and bacteria

Scientists at The University of Nottingham have discovered a key difference in the way our immune system responds to viral and bacterial pathogens.

A study published in the journal Nature Immunology and led by Professor Uwe Vinkemeier in the University's School of Life Sciences, centred on the STAT1 protein. STAT1 can bind DNA, therefore playing a vital role in regulating genes in the body.

STAT-1 responds to interferon signals — hormone-like molecules that control communication between cells — in order to trigger the body's immune defense against pathogens such as bacteria, viruses, or parasites. Our immune system also responds to malignant tumors to achieve their complete elimination.


It was previously thought that all interferons used single STAT1-containing units to regulate gene activity, rather than STAT1 chains.

However, using mice bred to express a mutated form of STAT1 that only forms single STAT1 units — the Nottingham team abolished the function of some interferons leaving others largely unaffected.

Researchers found that when the assembly of STAT1 chains was inhibited, type I interferons (responsible for protecting against viruses) were unaffected, but type II interferons (which protect against bacterial infections) no longer functioned.


Professor Vinkemeier said: "The core of these findings is that we are revising a central aspect of what we thought we knew about how these proteins worked. The molecular mechanisms underlying type I and type II interferon functioning are actually more distinct than we previously imagined. This in turn offers new options for pharmacological intervention."


Type I interferons involved in anti-viral response, also play a role in stopping cells from growing and replicating — therefore inhibiting the spread of the virus.

Type I interferons are already in clinical use against Hepatitis virus and several cancers and in the treatment of auto-immune diseases like multiple sclerosis.

Type-II interferon, in contrast, has been shown to be detrimental in use on some of these conditions, namely multiple sclerosis and melanoma, an aggressive type of skin cancer.


"In situations like these, our finding offer a new target for making current treatments more effective. There is good reason to assume that an inhibitor of STAT1 chain formation could potentially block detrimental type-II interferon responses while keeping type I activities, including anti-viral protection, intact. This would avoid an important shortcoming of current STAT1 inhibitors."

Abstract
STAT1 is an indispensable component of a heterotrimer (ISGF3) and a STAT1 homodimer (GAF) that function as transcription regulators in type 1 and type 2 interferon signaling, respectively. To investigate the importance of STAT1-cooperative DNA binding, we generated gene-targeted mice expressing cooperativity-deficient STAT1 with alanine substituted for Phe77. Neither ISGF3 nor GAF bound DNA cooperatively in the STAT1F77A mouse strain, but type 1 and type 2 interferon responses were affected differently. Type 2 interferon–mediated transcription and antibacterial immunity essentially disappeared owing to defective promoter recruitment of GAF. In contrast, STAT1 recruitment to ISGF3 binding sites and type 1 interferon–dependent responses, including antiviral protection, remained intact. We conclude that STAT1 cooperativity is essential for its biological activity and underlies the cellular responses to type 2, but not type 1 interferon.

The study was led by The University of Nottingham but involved international collaboration with researchers from Germany at the University of Göttingen Medical Centre and the Max-Planck Institute for Molecular Cell Biology and Genetics in Dresden; the Swiss Tropical and Public Health Institute in Basel, and the University of Vienna in Austria.

A copy of the paper can be found on the web at http://dx.doi.org/10.1038/ni.2794